Jenny Andreas, Darken Rachel S, Wilson Paul A, Mlodzik Marek
Mount Sinai School of Medicine, Brookdale Department of Molecular, Cellular and Developmental Biology, 1 Gustave L.Levy Place, New York, NY 10029, USA.
EMBO J. 2003 Sep 1;22(17):4409-20. doi: 10.1093/emboj/cdg424.
Frizzled (Fz) signaling regulates the establishment of planar cell polarity (PCP). The PCP genes prickle (pk) and strabismus (stbm) are thought to antagonize Fz signaling. We show that they act in the same cell, R4, adjacent to that in which the Fz/PCP pathway is required in the Drosophila eye. We demonstrate that Stbm and Pk interact physically and that Stbm recruits Pk to the cell membrane. Through this interaction, Pk affects Stbm membrane localization and can cause clustering of Stbm. Pk is also known to interact with Dsh and is thought to antagonize Dsh by affecting its membrane localization. Thus our data suggest that the Stbm/Pk complex modulates Fz/Dsh activity, resulting in a symmetry-breaking step during polarity signaling.
卷曲蛋白(Fz)信号通路调控平面细胞极性(PCP)的建立。PCP基因棘状蛋白(pk)和平行失常蛋白(stbm)被认为可拮抗Fz信号通路。我们发现它们在果蝇眼睛中与Fz/PCP通路所需细胞相邻的同一个细胞R4中发挥作用。我们证明Stbm和Pk存在物理相互作用,且Stbm将Pk招募至细胞膜。通过这种相互作用,Pk影响Stbm的膜定位并可导致Stbm聚集。已知Pk还与Dsh相互作用,并被认为通过影响其膜定位来拮抗Dsh。因此,我们的数据表明Stbm/Pk复合物调节Fz/Dsh活性,从而在极性信号传导过程中导致一个打破对称性的步骤。